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Increased Plasma Endothelin-1 in Pulmonary Hypertension: Marker or Mediator of Disease?

Duncan J. Stewart, MD; Robert D. Levy, MD; Peter Cernacek, MD; and David Langleben, MD
[+] Article, Author, and Disclosure Information

Grant Support: By grants from the Medical Research Council of Canada and the Quebec Heart Foundation; the Canadian Heart Foundation; and the Quebec Pulmonary Association.

Current Author Addresses: Dr. Stewart: Division of Cardiology, Room M4.76, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1.

Dr. Levy: Division of Respirology, Room L4.09, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1.

Dr. Cernacek: Division of Clinical Biochemistry, Room H7.22, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1.

Dr. Langleben: Division of Cardiology, S.M.B.D. Jewish General Hospital, 3755 Cote Ste Catherine, Montreal, Quebec H3T 1E2.

© 1991 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1991;114(6):464-469. doi:10.7326/0003-4819-114-6-464
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Objective: To explore the role of endothelin-1, a potent endothelial-derived vasoconstrictor peptide, in pulmonary hypertension, by measuring its concentration in arterial and venous plasma.

Design: A survey, case series study.

Setting: University-affiliated hospitals and outpatient clinics.

Patients: Twenty-seven patients with pulmonary hypertension: 7 with primary, and 20 with secondary pulmonary hypertension of various causes. The control groups (n = 16) comprised 8 healthy volunteers and 8 patients with coronary artery disease but without evidence of pulmonary hypertension.

Measurements and Main Results: Pulmonary artery pressure was markedly increased (94/43 ±23/13 mm Hg) in the patients with pulmonary hypertension. Venous plasma immunoreactive endothelin-1, measured by a specific radioimmunoassay, was significantly higher in patients with pulmonary hypertension (3.5 ±2.5 pg/mL, P < 0.001) than in normal subjects (1.45 ±0.45 pg/mL), or patients with coronary disease (0.75 ± 0.64 pg/mL). The arterialto-venous ratio of immunoreactive endothelin-1 was significantly greater than unity in primary pulmonary hypertension (2.21 ± 0.72, P = 0.01), whereas the patients with secondary pulmonary hypertension had a mean ratio not different from 1 (0.97 ± 0.42). In contrast, the mean arterial-to-venous ratios were significantly less than unity in both control groups (0.59 ± 0.35, and 0.54 ± 0.64; P < 0.02, for normal subjects and coronary disease patients, respectively), indicating a possible clearance of endothelin-1 across the healthy lung.

Conclusions: Patients with pulmonary hypertension have substantial alterations in plasma immunoreactive endothelin-1, which may reflect changes in net release or clearance of endothelin-1 by the lung. In patients with primary pulmonary hypertension, the high levels in arterial compared with venous plasma suggest pulmonary production of endothelin-1, which may contribute to elevated pulmonary vascular resistance.





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